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Cochlear cytokine gene expression in murine acute otitis media.

机译:小鼠急性中耳炎中耳蜗细胞因子基因的表达。

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OBJECTIVE: Recurrent acute otitis media (AOM) causes sensorineural hearing loss by unknown mechanisms. It is widely accepted that inflammatory cytokines diffuse across the round window membrane to exert cytotoxic effects. This study addresses whether inner ear cells are capable of expressing genes for inflammatory cytokines. STUDY DESIGN: The authors conducted a prospective animal study. METHODS: BALB/C mice underwent transtympanic injection of heat-killed Haemophilus influenzae to create an acute inflammatory response. These mice were compared with a control group in addition to a group of uninjected mice found to have otomicroscopic changes consistent with persistent or chronic otitis media. The cochleas of these mice were obtained, their RNA harvested, and cytokine gene expression analyzed using prefabricated cDNA arrays. RESULTS: Four groups of mice (control, 3-day postinjection, 7-day postinjection, and mice with chronic otitis media) with five mice in each group were analyzed. Numerous classes ofgenes were found to be upregulated or downregulated by more than twofold. Some genes differed from control mice by more than 10-fold. These genes included numerous fibroblast growth factors, interleukins, tumor necrosis factors, and colony-stimulating factors. CONCLUSION: The genes of numerous inflammatory cytokines are either up- or downregulated by murine inner ear cells in response to either acute or chronic inflammation of the middle ear. This study provides a novel site of production of cytokines that may be responsible for the damage seen in sensorineural hearing loss.
机译:目的:复发性急性中耳炎(AOM)通过未知机制引起感觉神经性听力丧失。炎症细胞因子在整个圆窗膜上扩散以发挥细胞毒性作用已被广泛接受。这项研究解决了内耳细胞是否能够表达炎性细胞因子的基因。研究设计:作者进行了一项前瞻性动物研究。方法:对BALB / C小鼠进行鼓膜注射热杀死的流感嗜血杆菌,以产生急性炎症反应。将这些小鼠与对照组进行比较,除了一组未注射的小鼠,发现其具有与持续性或慢性中耳炎一致的耳镜变化。获得这些小鼠的耳蜗,收获它们的RNA,并使用预制的cDNA阵列分析细胞因子基因的表达。结果:分析了四组小鼠(对照组,注射后3天,注射后7天和患有慢性中耳炎的小鼠),每组五只小鼠。发现许多种类的基因被上调或下调两倍以上。一些基因与对照小鼠的差异超过10倍。这些基因包括许多成纤维细胞生长因子,白介素,肿瘤坏死因子和集落刺激因子。结论:小鼠内耳细胞响应中耳的急性或慢性炎症,会上调或下调多种炎症细胞因子的基因。这项研究提供了一种新的细胞因子产生位点,其可能与感觉神经性听力损失中的损害有关。

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